Much of the heart consists of a special type of muscle called myocardium. The myocardium requires a constant supply of oxygen and nutrients to allow it to contract and pump blood throughout the vasculature. One method of improving reduced myocardial blood supply is called transmyocardial revascularization (TMR), the creation of pathways or channels into the myocardium generally from either an outer epicardial surface of the heart in a surgical procedure or from an inner endothelium cell covered surface of a heart's endocardium chamber in a percutaneous transluminal myocardial revascularization (PTMR).
A procedure using needles in a form of myocardial acupuncture was used clinically in the 1960s. Deckelbaum. L. I., Cardiovascular Applications of Laser Technology, Lasers in Surgery and Medicine 15: 315-341 (1994). The technique was said to relieve ischemia by allowing blood to pass from the ventricle through the channels either directly into other vessels perforated by the channels or into myocardial sinusoids which connect to the myocardial microcirculation. These sinusoidal communications vary in size and structure, but represent a network of direct arterial-luminal, arterial-arterial, arterial-venous, and venous-luminal connections. Interest in myocardial acupuncture or boring, which mechanically displaces or removes tissue, decreased when it was discovered that the mechanically created channels closed because of acute thrombosis followed by organization and fibrosis of clots.
By contrast, recent histological evidence of patent, endothelium-lined tracts within pathways created with laser energy supports the assumption that the lumen of the laser pathways is or can become hemocompatible and resist occlusion caused by thrombo-activation and/or fibrosis. A thin one of charring occurs on the periphery of the laser-created transmyocardial channels through the well-known thermal effects of optical radiation on cardiovascular tissue. This type of interface may inhibit the immediate activation of the intrinsic clotting mechanisms because of the inherent hemocompatibility of carbon. In addition, the precise cutting action that results from the high absorption and low scattering of laser energy (CO.sub.2, Ho, etc.) may minimize structural damage to collateral tissue, thus limiting the tissue thromboplastin-mediated activation of extrinsic coagulation. Recent histological studies show that both patent and non-patent channels promote growth of an alternate circulation, one of the mechanisms believed to be beneficial following the procedure.
Despite the creation of patent channels and pathways with lasers, there are reported problems associated with laser TMR procedures. Such problems can include channel closure which may be caused by selection and use of TMR laser parameters which do not produce channels with the characteristics detected in the histological evidence discussed above. An additional reported problem encountered in TMR procedures is adverse effects created by the laser on the diseased hearts of TMR patient's.
U.S. Pat. No. 4,658,817 issued Apr. 21, 1987 to Hardy teaches a method and apparatus for TMR using a surgical CO.sub.2 laser including a handpiece for directing a laser beam to a desired location. Hardy suggests that the creation of TMR channels using a laser may affect contractility of the heart and states that the number of perforations may have to be limited accordingly.
Two subsequent patents, U.S. Pat. Nos. 5,380,316 issued Jan. 10, 1995 and 5,389,096 issued Feb. 14, 1995 both to Aita et al., discuss in general methods for intra-operative and percutaneous myocardial revascularization, respectively. Both patents suggest synchronization of the laser with the heart beat is necessary to avoid arrhythmias. PCT WO 96/35469 issued Nov. 14, 1996 to Aita et al. also discusses apparatus and general methods for percutaneous myocardial revascularization synchronized with the heart beat to avoid arrhythmias.
Synchronization of the laser energy delivery with the beating of the heart was also considered an important tool in U.S. Pat. No. 5,125,926 issued Jun. 30, 1992 to Rudko et al., reportedly to reduce the chance of laser induced fibrillation. Rudko et al teaches a heart-synchronized pulsed laser system for TMR. Utilizing electrical sensing, the heart beat is monitored using an EKG device. The device automatically delivers what appears to be a square pulse of laser energy to the heart only in response to electrical detection of a predetermined portion of the heartbeat cycle.
The prior art discussed above suggests that at least some pulsed laser systems and parameters are potentially damaging to the beating heart or its action and may induce fibrillation or arrhythmia, hence the need for heart synchronization to minimize such effects.
An arrhythmia is a disturbed heart rhythm which often takes over as the primary rhythm of the heart, as evidenced by a rapid flutter or other rhythm of the heart muscle, which renders it ineffective at pumping blood through the vasculature. The process of delivering laser energy to tissue results in polarization of individual cells of the heart in the area of delivery of the laser energy. Polarization of the specialized conducting cells as well as myocardial cells drives the action potential of cells resulting in responsive contractile motion. Delivering laser energy can disrupt the normal rhythm of the heartbeat since the cardiac rhythm can be side-tracked to that of the polarized cells as opposed to propagating through the heart along the normal path of the impulse.
The heart's natural, primary pacemaker is found in a group of cells called the sinoatrial or sinus node located near the junction of the superior vena cava and the right atrium. The electrical impulse originates in the endocardium and propagates through the myocardium to the epicardial surface. The electrical impulse is conducted out of the sinus node to the atria, where it stimulates atrial muscle cells to contract, and to the atrioventricular node. Upon leaving the atrioventricular node, the electrical impulse continues to propagate down the conducting system to the bundle of His, into right and left branches thereof. The right bundle spreads the electrical impulse to the right ventricle and the left bundle branch propagates the impulse to anterior and posterior positions in the left ventricle to reach the Purkinje fibers. These small fibers form a rapid conduction network through the myocardium to deliver the impulse to all of the individual contractile muscle cells of the myocardium.
The electrical signal travels at different speeds at different parts of the network. While electrical signals on the portion of the network extending through the atria have been found to travel at velocities of about 1 meter per second, these signals slow to about 0.2 m/s as they pass through the atrioventricular node. Signal propagation through the ventricular Purkinje network, however, is much faster--approximately 4 n/s. Thus, the sinus node is responsible for producing a repeating electrical impulse which ultimately causes the muscle cells of the heart to contract in repetitive, wave-like convulsions.
The synchronization solutions proposed in the prior art discussed above do not address methods for detecting and compensating for hard to detect, abnormal conduction patterns or rhythms which may occur in damaged hearts. Additionally, EKG monitoring may not detect and allow compensation for localized or isolated areas of heart tissue which may not be synchronized with other areas of heart tissue. Excitation of such isolated areas may cause arrhythmias. In addition to the problems discussed above, heart synchronization as described in the prior art limits the amount of time the laser can be activated during a heart cycle, thereby increasing the time of a TMR procedure.
A need exists in the prior art for a method and apparatus for performing TMR and PTMR procedures quickly using specified laser parameters selected to minimize possible cardiac arrhythmias without the need for monitoring the heart beat.